AVP is known to enhance hepatic glycogenolysis by activation of V1a receptors and by increasing the release of glucagon, resulting in increased glucose levels in experimental animals. Even when glucagon receptors in the liver are blocked, AVP still increases blood glucose. The V1b receptors have been identified in both alpha and beta cells of the islets of Langerhans. Thus, AVP stimulates insulin secretion counteracting the increase in blood glucose. In an experiment with AVP V1a and V1b receptor knockout mice, alterations in glucose and fat metabolism were observed, suggesting that AVP might play a role in glucose regulation and metabolic disorders. Studies in humans with a genetic variation of AVP V1a receptor showed increased prevalence of diabetes in overweight or subjects with high fat diet. Recently, a study in rats prone to metabolic dysfunction, examined the effect of long-term influence of vasopressin on glucose homeostasis. It reported that high vasopressin enhanced hyperinsulemia and glucose intolerance in obese rats, while treatment with vasopressin receptor V1a antagonist reduced glucose intolerance.